The specific aim of this proposed project is to develop tecniques for minimizing the degree of myocardial injury associated with the use of ischemic arrest during cardiopulmonary bypass. Operating on a bloodless, flaccid, nonbeating, arrested heart, facilitates repairs of cardiac defects or completion of a delicate anastomosis. Such cardiac arrest, while diminishing oxygen demand, reduces or eliminates myocardial oxygen supply and substrate replenishment, rapidly causing myocardial ischemia. A well-described technique termed cardioplegia has been developed to prevent myocardal infarction occurringduring this ischemic process. A cardioplegic solution is one which induces cardiac arrest (a cessation of mechanical and electrical activity) when coming into contact with the myocardial cell through the coronary vascular bed. The overall objectives of his research project are to evauate different cardioplegic solutions (primarily based on magnsium and potassium) in order to help establish the best solution for clinical use. In addition, following a period of ischemic arrest, whether cardioplegic is employed or not, myocardial reperfusion has been shown to occasionally induce untoward metabolic effects and promote myocardial edema leading to cell injury, despite the completion of the ischemic process. An additional important objective is to attempt to define this myocardial reperfusion injury and to achieve a means of offsetting it. The experimental method involves studying myocardial viability by cellular high-energy phosphate and enzyme measurements, evaluating myocardial function, determining the level of myocardial perfusion before and after ischemia, and evaluating electron microscopic examination of the heart muscle.